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Royal Jelly Abrogates Cadmium-Induced Oxidative Challenge in Mouse Testes: Involvement of the Nrf2 Pathway
Rafa S Almeer1, Doaa Soliman2, Rami B Kassab3
1Department of Zoology, College of Science, King Saud University, Riyadh 11495, Saudi Arabia. ralmeer@ksu.edu.sa.
Abstract:
The current study examined the efficacy of royal jelly (RJ) against cadmium chloride (CdCl₂)-induced testicular dysfunction. A total of 28 Swiss male mice were allocated into four groups (n = 7), and are listed as follows: (1) the control group, who was intraperitoneally injected with physiological saline (0.9% NaCl) for 7 days; (2) the RJ group, who was orally supplemented with RJ (85 mg/kg daily equivalent to 250 mg crude RJ) for 7 days; (3) the CdCl₂ group, who was intraperitoneally injected with 6.5 mg/kg for 7 days; and (4) the fourth group, who was supplemented with RJ 1 h before CdCl₂ injection for 7 days. Cd-intoxicated mice exhibited a decrease in serum testosterone, luteinizing hormone (LH), and follicle stimulating hormone (FSH) levels. A disturbance in the redox status in the testicular tissue was recorded, as presented by the increase in lipid peroxidation and nitrate/nitrite levels and glutathione (GSH) depletion. Moreover, the activities of glutathione peroxidase (GPx), glutathione reductase (GR), superoxide dismutase (SOD), catalase (CAT), and nuclear factor (erythroid-derived 2)-like-2 factor (Nrf2) and their gene expression were inhibited. In addition, interleukin-1ß (IL-1β) and tumor necrosis factor-α (TNF-α) levels were elevated. Furthermore, Cd triggered an apoptotic cascade via upregulation of caspase-3 and Bax and downregulation of Bcl-2. Histopathological examination showed degenerative changes in spermatogenic cells, detachment of the spermatogenic epithelium from the basement membrane, and vacuolated seminiferous tubules. Decreased cell proliferation was reflected by a decrease in proliferating cell nuclear antigen (PCNA) expression. Interestingly, RJ supplementation markedly minimized the biochemical and molecular histopathological changes in testes tissue in response to Cd exposure. The beneficial effects of RJ could be attributed to its antioxidative properties.
Insights
Royal jelly (RJ) protects against cadmium chloride (CdCl₂) induced testicular dysfunction in mice. RJ supplementation mitigated CdCl₂-induced oxidative stress, inflammation, apoptosis, and histopathological damage in testes.
Area of Science:
- Toxicology
- Reproductive Biology
- Natural Product Research
Background:
- Cadmium chloride (CdCl₂) is a toxic heavy metal known to induce testicular dysfunction.
- Oxidative stress, inflammation, and apoptosis are key mechanisms underlying CdCl₂-induced testicular damage.
- Royal jelly (RJ), a natural product, possesses antioxidant and anti-inflammatory properties.
Purpose of the Study:
- To investigate the protective effects of royal jelly (RJ) against cadmium chloride (CdCl₂)-induced testicular toxicity in male mice.
- To evaluate the impact of RJ on hormonal levels, redox status, inflammatory markers, and apoptotic pathways in CdCl₂-exposed testes.
- To assess the histopathological changes and cell proliferation in testes following CdCl₂ exposure and RJ treatment.
Main Methods:
- Male Swiss mice were divided into four groups: control, RJ-treated, CdCl₂-intoxicated, and RJ + CdCl₂-treated.
- CdCl₂ was administered intraperitoneally, while RJ was given orally for seven days.
- Serum hormone levels, testicular redox status (lipid peroxidation, GSH), antioxidant enzyme activities (GPx, GR, SOD, CAT), Nrf2 expression, inflammatory cytokines (IL-1β, TNF-α), apoptotic markers (caspase-3, Bax, Bcl-2), and PCNA expression were analyzed.
- Histopathological examination of testicular tissue was performed.
Main Results:
- CdCl₂ exposure significantly decreased serum testosterone, luteinizing hormone (LH), and follicle stimulating hormone (FSH) levels.
- CdCl₂ intoxication induced oxidative stress, evidenced by increased lipid peroxidation and nitrate/nitrite, and decreased glutathione (GSH) levels.
- Activities and gene expression of antioxidant enzymes (GPx, GR, SOD, CAT) and Nrf2 were significantly inhibited by CdCl₂.
- CdCl₂ elevated pro-inflammatory cytokines (IL-1β, TNF-α) and triggered apoptosis via caspase-3 and Bax upregulation, and Bcl-2 downregulation.
- Histopathological analysis revealed degenerative changes in seminiferous tubules and decreased cell proliferation (PCNA).
- RJ supplementation markedly ameliorated all the observed CdCl₂-induced biochemical, molecular, and histopathological alterations.
Conclusions:
- Royal jelly (RJ) exhibits significant protective effects against cadmium chloride (CdCl₂)-induced testicular dysfunction in male mice.
- RJ's beneficial actions are attributed to its potent antioxidant properties, which counteract CdCl₂-induced oxidative stress and inflammation.
- RJ supplementation can mitigate CdCl₂-induced hormonal imbalance, apoptosis, and histopathological damage, preserving testicular integrity and function.
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